Kupffer cell depletion attenuates superoxide anion release into the hepatic sinusoids after lipopolysaccharicle treatment]

Masahiko Fukuda, Hirokazu Yokoyama, Takeshi Mizukami, Hideki Ohgo, Yukishige Okamura, Yoshitaka Kamegaya, Yoshinori Horie, Shinzo Kato, Hiromasa Ishii

Research output: Contribution to journalArticle

22 Citations (Scopus)


Background and Aim: The mechanisms involved in the beneficial effect of gadolinium chloride against endotoxin-induced liver damage were studied. Methods: Superoxide anions released into the hepatic sinusoids were examined in a liver perfusion model using the cytochrome C method. Results: Gadolinium chloride treatment fully depleted ED2-positive cells from the liver and significantly attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-α (TNF-α) challenge. Moreover, gadolinium chloride treatment resulted in a significant decline in endothelial cell damage in the hepatic sinusoids as assessed by the purine nucleoside phosphorylase/glutamic-pyruvic transaminase ratio in the liver perfusate. Although gadolinium chloride treatment did not affect the level of serum TNF-α, it significantly reduced that of interleukin (IL)-8 and neutrophil migration in the hepatic sinusoids after the lipopolysaccharide challenge. Conclusion: These data suggest that a reduction of the superoxide anion level in the hepatic sinusoids in acute endotoxemia and subsequent reduction of neutrophil migration into the liver may indicate that gadolinium chloride treatment suppresses the progression of liver damage in acute endotoxemia.

Original languageEnglish
Pages (from-to)1155-1162
Number of pages8
JournalJournal of Gastroenterology and Hepatology (Australia)
Issue number10
Publication statusPublished - 2004 Oct



  • Free radical
  • Kupffer cell
  • Macrophages
  • Neutrophils

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology

Cite this